Studies of non-human animals have provided ample evidence that opioids are involved in reward processes. Less is known about the role of the opioid system for human reward processes. We hypothesized that an opioid agonist would increase, and an opioid antagonist would decrease responsiveness to rewards in healthy humans. We tested 30 healthy male participants on a reward responsiveness task using a randomized, placebo-controlled double-blind design. Participants received oral treatment with a µ-opioid agonist (morphine, 10mg), a non-selective opioid antagonist (naltrexone, 50mg) or placebo on three separate days. One-two hours after drug administration, one of three locally developed versions of a reward responsiveness task was completed. The task was a two-alternative signal detection task with a skewed reward schedule. Stimuli were schematic faces which differed in the size or position of the mouth. Reward responsiveness was operationalized as a bias towards choosing the most frequently rewarded response option. In line with our hypothesis, the results showed that morphine significantly increased and that naltrexone significantly decreased bias relative to placebo. These effects could be due to either a direct effect of opioid agonism/antagonism on the neural reward system, or due to indirect effects, e.g. via opioid effects on striatal dopamine functioning. Notably, although our naltrexone condition would be expected to block endogenous opioid function, reward responsiveness was not completely eliminated. This could indicate that opioids may be involved in, but not necessary for, this effect. Overall, our findings confirm a role for the opioid system in human reward responsiveness.